IntroductionWe tested the extent to which the catechol‐O‐methyltransferase (COMT) Val158Met polymorphism is associated with affective state and evening cortisol levels. We limited our study to women as previous research suggests that the link between COMT genotype and psychological health is entangled by sex differences.Materials and MethodsThe participants were assessed on measures of anxiety, mood disturbance, depressive symptomatology, and perceived stress. We also evaluated participants on a quality of life measures that included two emotion domains and two physical domains (physical health and environment).ResultsWe found that under normal (nonstress) conditions, the COMT A allele (Met carriers, higher dopamine) associates with healthier affect and lower afternoon cortisol levels in women. These effects were limited to affective measures and not to physical or environmental quality of life.ConclusionsThese findings help to shed light on the complex nature of COMT and emotion, and suggest that both sex and task condition (stress vs. nonstress) should be considered when examining the relationship between COMT genotype and emotion.

Chronic sleep deprivation has been demonstrated to diminish cognitive performance, alter mood states, and concomitantly dysregulate inflammation and stress hormones. At present, however, there is little understanding of how an acute sleep deprivation may collectively affect these factors and alter functioning. The present study aimed to determine the extent to which 24-h of sleep deprivation influences inflammatory cytokines, stress hormones, cognitive processing across domains, and emotion states. To that end, 23 participants (mean age = 20.78 years, SD = 2.87) filled out clinical health questionnaires measured by the Pittsburgh Sleep Quality Index, Morningness Eveningness Questionnaire, and Center for Epidemiological Studies Depression Scale. Actigraph was worn for seven days across testing to record sleep duration. At each session participants underwent a series of measures, including saliva and blood samples for quantification of leptin, ghrelin, IL-1β, IL-6, CRP, and cortisol levels, they completed a cognitive battery using an iPad, and an emotion battery. We found that an acute sleep deprivation, limited to a 24 h period, increases negative emotion states such as anxiety, fatigue, confusion, and depression. In conjunction, sleep deprivation results in increased inflammation and decreased cortisol levels in the morning, that are accompanied by deficits in vigilance and impulsivity. Combined, these results suggest that individuals who undergo 24 h sleep deprivation will induce systemic alterations to inflammation and endocrine functioning, while concomitantly increasing negative emotions.

Introduction: A large and growing body of evidence shows that sleep loss has profound deleterious effects on health and has been specifically linked to the development of several cancers. Despite this obvious health cost, there is almost no current understanding of how sleep loss increases the risk for tumor development. The purpose of the present study was to identify epigenetic mechanisms through which total sleep deprivation (TSD) altered expression of known cancer-related genes (suppressors and promoters). To that end, we tested the effects of TSD on the expression of miRNAs that are associated with tumor development. Methods: Twenty-three participants (14 males, mean age = 20) underwent actigraphy-verified TSD for 24 hours in a controlled environment. miRNA preparations were extracted from participants' plasma and processed for cDNA synthesis. The resulting cDNA pools were used as templates in qPCR reactions in an effort to estimate differential miRNA expression. Results: Results indicated that sleep deprivation caused significant differential expression of several specific miRNA tumor-related genes, including miR-15a, miR-96, and miR-296-5p. Accordingly, further tests were focused on these two miRNA species on a subset of participants. Results showed that, there was a significant upregulation of miR-15a (p < 0.05), miR-96 (p < 0.05), and miR-22 (p < 0.05), but not miR-296-5p (p=0.12). Conclusion: Overall, these findings show how even short-term sleep loss can alter cancer-associated pathways. Increased expression of miR-15a and miR-22 have known tumor suppression properties. It is possible that miR-15a and miR-22 exert protective effects in response the TSD-induced disruption to homeostasis. Although miR-96 is a known oncogene, it is also part a complex clock gene signaling pathway with diurnal expression. Accordingly, TSD potentially disrupts the normal diurnal expression pattern miR-96. We are currently following up on these results in a study of people who regularly experience sleep loss (i.e. chronic sleep restriction). Support (If Any):This work is supported by the Department of Education. Number P120A1400. INTERMITTENT HYPOXIA PARTIALLY IMPAIRS INSULIN-SIGNALING VIA INCREASES IN CAVEOLIN-1 EXPRESSION: VASCULAR IMPLICATIONSSingh P, Sharma P, Peterson TE, Zhang Y, Somers VK Mayo Clinic, Rochester, MN Introduction: Insulin resistance and endothelial dysfunction are associated with obstructive sleep apnea (OSA), which is characterized by frequent episodes of nocturnal intermittent hypoxia (IH). However, molecular mechanisms contributing to endothelial dysfunction and insulin resistance in OSA are not completely understood. Caveolin-1 (cav-1) is a membrane protein which negatively regulates endothelial nitric oxide synthase (eNOS) activity and contributes to endothelial dysfunction. The objective of our study was to examine the interactions between IH, cav-1, and eNOS activity in vascular endothelial cells in the context of insulin resistance. Methods: We used an in-vitro approach to examine the effects o...

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